GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE264nnn/GSE264595/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE264595GEOGSEfalseThe XPO7-NPAT axis represents key vulnerabilities in TP53-mutated acute myeloid leukemia (RNA-Seq)Mutation of TP53, a tumor suppressor in cancer, is common and leads to extremely poor prognosis. To identify vulnerabilities in TP53-mutated tumors, we performed genome-wide CRISPR/Cas9 screens using isogenic Trp53 wild-type and knockout mouse acute myeloid leukemia (AML) lines. Here, we show that histone gene regulation governed by the XPO7-NPAT pathway is essential for survival of TP53-mutated AML cells. In TP53 wild-type cells, XPO7 enhances p53 nuclear localization and functions as a tumor suppressor, but in TP53-mutated cells, XPO7 promotes cell proliferation by retaining NPAT, a histone gene activator, in the nucleus. NPAT depletion led to genome-wide histone loss, enhancing vulnerability to genotoxic stress. Human AML cases show predominant expression of XPO7 and NPAT when TP53 is mutated, suggesting a potential therapeutic vulnerability.2026/04/22GSE264595GSM8223530GSM8223531GSM8223520GSM8223532GSM8223521GSM8223533GSM8223522GSM8223534GSM8223523GSM8223524GSM8223535GSM8223536GSM8223525GSM8223537GSM8223526GSM8223527GSM8223528GSM822352921626264595Mus musculus